In patients with thrombocytopenia, sCD40L levels were clearly influenced by PLT transfusions: PLT administration led to a normalization of sCD40L plasma concentration. Nevertheless, adverse transfusion reactions did not occur in these patients. The sCD40L release capacity was enhanced by PLT administration dependent on the increase in the amount of PLT count.
Introduction: Soluble CD40L (sCD40L) is expressed by platelets and is involved in the stabilization of arterial thrombi. Additionally, it was shown that sCD40L accumulation occurred in stored blood products triggering adverse transfusion reactions like TRALI. To study the influence of the preparation technique on sCD40L accumulation and platelet function we examined CD40L concentrations in prestorage pooled platelet concentrates compared to apheresis products. In addition, sCD40L release capacity was determined as a marker for platelet viability.Material and methods: sCD40L concentrations were determined in prestorage pooled platelet concentrates (n = 8) and in platelet apheresis concentrates (n = 8) before and after platelet stimulation (recalcification and clot formation) at day 1, 3 and 5 under routine storage conditions. sCD40L concentrations were determined by a commercially available ELISA kit.Results: sCD40L concentrations in storage medium increased over time in prestorage pooled platelet concentrates (from 1,185 pg/mL ± 87 pg/mL at day 1 to 4,464 pg/mL ± 212 pg/mL at day 5) as well as in apheresis products (from 581 pg/ mL ± 124 pg/mL at day 1 to 2,718 pg/mL ± 154 pg/mL at day 5) in a hyperbolic manner. Recalcification and clot formation caused an increase in sCD40L concentrations (for example 3,842 pg/mL ± 769 pg/mL before platelet activation to 31,219 pg/mL ± 2,063 pg/mL after platelet activation at day 3), and we observed comparable release capacities for both preparation techniques, however, decreasing over storage time up to 50% (day 5) of the respective control value (day 1).Conclusions: Amounts of sCD40L accumulation and release capacity during storage of platelet concentrates were dependent on storage duration, but showed no relevant differences regarding the preparation technique. After 5 days of storage, CD40L basal levels were increased, in contrast sCD40L release capacity was decreased. By recalcification and clot formation sCD40L release capacity could be easily induced and is assumed to be used as a marker for platelet viability.
donor screening with cobas 201/cobas TaqScreen MPX under routine conditions at German Red Cross institutes. Vox Sang 2010;98:37-46. Soluble CD40 ligand in stem cell products of autologous donors_ 2916 226..228To the editor: To further the observations by Woods and colleagues 1 regarding cytokine levels in stem cell components, we would like to present our observations of soluble CD40 ligand (sCD40L) levels during peripheral stem cell apheresis in four autologous donors. Stem cell units contain a considerable amount of platelets (PLTs) that is variable by apheresis technique. PLTs are the major source of sCD40L 2 in the blood. It is known that there is an association between adverse transfusion reactions after PLT transfusions and the concentration of sCD40L. 3 Thus it may be helpful to define the amounts of sCD40L that accumulate in other blood components.The shedding process of sCD40L from the surface of activated PLTs is triggered by matrix metalloproteinase-2 (MMP-2), 4 and high concentrations of sCD40L can be observed in PLT concentrates stored at room temperature. 5 In four patients suffering from multiple myeloma and undergoing autologous stem cell apheresis, sCD40L concentrations were measured in peripheral blood samples before, during, and after an apheresis stem cell collection procedure and in the derived stem cell unit. sCD40L concentrations were determined by a commercially available enzyme-linked immunosorbent assay kit (R&D Systems, Minneapolis, MN). In an additional approach, the release of sCD40L was examined in PLT-rich plasma (PRP) derived from whole blood donations from healthy volunteers (n = 6) stored under different temperatures (4 and 37°C) for 30 minutes.During stem cell apheresis, a decrease in PLT count could be observed from 94,822 Ϯ 56,734/mL at the beginning to 75,134 Ϯ 25,678/mL (during stem cell collection) and to 55,007 Ϯ 26,567/mL at the end of the procedure (p < 0.05, t test). This PLT loss was accompanied by a significant lowering of sCD40L concentrations in peripheral blood samples from 241 Ϯ 137 pg/mL at the beginning to 192 Ϯ 91 pg/mL (during stem cell collection) and to 124 Ϯ 73 pg/mL at the end of the procedure (p < 0.05, t test, correlation coefficient r = 0.9 corresponding to the PLT count). In the stem cell units collected, the PLT count ranged from 938 ¥ 10 9 to 2976 ¥ 10 9 /L, and sCD40L concentrations were elevated substantially above peripheral blood levels to 2847 Ϯ 398 pg/mL (range, 2189 to 3641 pg/mL; p < 0.05 compared to peripheral blood). In PRP from healthy volunteers, sCD40L showed a significant increase at 37°C from 106.3 Ϯ 40.3 to 210.9 Ϯ 46.8 pg/mL (a 98% increase) after 30 minutes (p < 0.05). In contrast, at 4°C storage, no significant difference occurred (96.3 Ϯ 46.7 to 119.1 Ϯ 53.9 pg/mL).With these facts we want to give an additional comment to interpret the behavior of sCD40L in stem cell concentrates. In support of the observations of Woods and colleagues, 1 our data show a slow release of sCD40L at 4°C. This may be attributable to reduced activity un...
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